A total of 321 patients hospitalized in Guangxi Medical University Affiliated Tumor Hospital from November 2013 to December 2017 who were pathologically or cytologically confirmed NSCLC with malignant pleural effusion (MPE) were enrolled in the study. The information including clinical features at baseline, pleural effusion status, EGFR genomic alternation, treatment and prognosis for patients were retrospectively extracted and analyzed. The data were analyzed by SPSS 21.0 software. Chi-square test was used for comparison between groups, and Fisher’s exact probability method was used for correction. Survival curves were drawn by Kaplan-Meier method, and the differences between groups were compared by log-rank test. P < 0.05 was considered as statistical significance.

Through comparing clinicopathological characteristics, EGFR genotyping and prognosis in MPE patients, those whose MPE were identified at the time of diagnosis are more frequently a higher incidence of ECOG score and bone metastasis, a longer OS in patients with EGFR mutation and treated with EGFR-TKI, and a significantly lower OS in patients with wild-type EGFR and liver metastasis.

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137P - Detection and clinicopathologic features of ctDNA in T790M-positive advanced lung adenocarcinomas patients after failure of treatment with first- and second-generation EGFR-TKIs (ID 359)

We aimed to detect ctDNA in patients with advanced lung adenocarcinomas after failure of treatment with first- and second-generation EGFR-TKIs and to analyze it’s clinicopathologic features in a subset of patients harbouring the T790M mutation.

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Methods

We retrospectively collected data from November 2016 to October 2018 in patients with lung adenocarcinomas who had been analysed by Next-Generation Sequencing or ddPCR after progression on EGFR-TKIs at GuangXi Medical University Affiliated Tumor Hospital. Statistical analyses were performed to examine the associations between clinicopathologic features and acquired T790M mutation in patients.

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Results

A total of 72 plasma samples were collected, of which 17 had matched tissue biopsies. Of these patients, 48 were analysed by NGS and the rest by ddPCR. The T790M mutation was detected in 43 cases (59.7%). We found this mutation was higher than that of mPFS>11.5 months (79% vs. 44%; odds ratio, 4.516; 95%CI, 1.53 to 13.30; p=0.006), and in which longer median PFS (13.0 months vs. 9.0 months; p = 0.042). Those who received chemotherapy before EGFR-TKIs were more likely to have the T790M mutation (80% vs. 53%, p=0.03) compared to those who received EGFR-TKIs in the first-line. In this study, the occurrence of T790M mutation in patients with L858R mutation was higher than seen in patients with 19-del (65% vs.57%; p=0.809). Among 17 patients who were sequenced by NGS in both samples, 7 had T790M positive blood samples and 8 were T790M positive in tissue biopsies. The coincidence rate was 94%.10 cases after the progression of the third generation TKI treatment. Three cases of T790M with C797S cis-mutation were detected and 3 cases with PIK3CA, BRAF V600E and MAP2K1 mutations, respectively. Secondary resistance mutations were not detected by NGS in 4 cases.

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Conclusions

Patients with advanced lung adenocarcinomas harbouring the T790M mutation who failed with first- or second-generation EGFR-TKIs were more likely to have longer mPFS. In this study, NGS testing using ctDNA was a feasible means for monitoring acquired resistance mutations during or after progression on targeted therapy.

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